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How very Texas.

Another possibility is that the means are estimated at T1 and T2 because the true means cannot be calculated due to dropouts (but they can be calculated at baseline). This is apparently what intention-to-treat analysis deals with.

This is the key part of the text explain the method to achieve the values in Table 3. It seems convoluted to me, and perhaps these numbers are 'modelled'. But, if this is the case, why not just use the actual values!

One question I have: the title says 'Estimated means and linear mixed model analyses....' What do they mean by this? Are they showing results from some extra modeling step? EDIT: And why are T1 and T2 means referred to as 'Estimated means', whereas the baseline value at T0 is just 'mean'...

If it's not too much trouble, @ME/CFS Skeptic, are you able to resend this image with the repeated SEs at T0 also highlighted. There is one instance. Cheers.

This is used to calculate the error on the between-group difference. The SE we have flagged are on individual groups (i.e., calculated before that stage), so this shouldn't matter.

I did think of doing the latter. I just don't want to take liberties.

Yep the SD would be 3.775 for CIS-fatigue in the CBT group (SE=0.5), much lower than 12.

No, we need more research on the biological basis of stress and its interaction with the immune system, particularly in the brain.

PS I would really like to know if the first point—about the repetitive standard error values in Table 3—can be explained, if there's anyone here with a good background in clinical stats...

Yesterday, I sent some comments to Hans Knoop and Tanja Kuut on potential issues with the data in Table 3 and presentation of results in Fig 2. I have asked that they consider addressing these points—which may well be explainable—before the paper is published in final form. Lets see if they do...

One of my comments is on this topic. The answers to infection type are 'baked-in' to the questionnaire, so now you can't subset by e.g., enteroviruses. Having said that, glandular fever is relatively easier to confirm in the clinic.

Here are some (mostly minor) comments from me. I will also send these to the lead author.

Another great blog, Michiel. Have you considered submitting this to a journal as a sort of comment / view piece? It is definitely good enough.

"The solution presented is a Belgian compromise, one that everyone can live with but that makes no sense at all." Exactly. I did not know this term existed, but it captures the situation well.

The deconditioning and exercise avoidance hypotheses were *foundational* in the justification for ME-CBT and ME-GET. If you remove them, the whole house of cards collapses. They've really got themselves in a muddle, and patients will be better of if the BPS lot just admitted as much.

i agree. I think at some point there will be a reckoning, but for now the preliminary links between our environment and (chronic) illness are being treated as inconvenient truths.

Some recent posts in another thread reminded me of this paper. I'm suprised this has not been published yet. A tweet in the thread from the journalist who originally shared these snippets says "due to be published soon in the Journal of Neurology, Neurosurgery, and Psychiatry." That appears...

"Our foundation supports nationally and internationally recognized research projects, non-profit organizations to support those affected and charity projects to combat diseases such as myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) and related diseases. "We can build on a network...